摘要
目的研究肺炎克雷伯杆菌对氟喹诺酮类药物(FQNs)的耐药机制。方法筛选临床分离的对环丙沙星耐药的肺炎克雷伯杆菌共10株,采用微量肉汤稀释法检测菌株对5种氟喹诺酮类药物的MIC值;采用PCR方法检测菌株染色体和质粒携带的喹诺酮耐药基因(gyrA基因、parC基因和qnr基因)并测序;质粒接合试验验证qnr基因的转移性。结果 10株肺炎克雷伯杆菌对5种氟喹诺酮类药物均产生耐药性。扩增产物经测序发现10株肺炎克雷伯杆菌染色体的gyrA基因和parC基因均有突变;有2株菌株(K79和K107)携带qnrA基因,这2株菌的接合菌对喹诺酮抗菌药的MIC值上升了5～30倍;未检测到qnrB阳性的菌株。结论 gyrA和parC基因突变是肺炎克雷菌对氟喹诺酮类产生耐药机制的主要原因,质粒上qnrA基因的存在,也是产生喹诺酮耐药的一个重要因素。
Objective To investigate the mechanisms of the resistance of Klebsiella pneumoniae（K.pneumoniae） to Fluoroquinolones（FQNs）.Method 10 FQNs-resistant K.pneumoniae strains were isolated clinically.Minimal inhibitory concentrations（MIC） against the 5 FQNs were determined with the broth microdilution method.FQNs-resistant genes were detected with polymerase chain reaction（PCR） and the products were sequenced.The qnr gene transferability in vitro was verified by conjugation experiments.Result All the strains of K.pneumoniae were resistant to the FQNs.The results of DNA sequencing showed that all strains had gyrA and parC gene mutation.Two strains（K79 and K107） carried qnrA gene.Their MICs of FQNs were increased by 5 to 30 folds.The qnrB gene was not detected.Conclusion Mutation of gyrA and parC gene is the primary mechanism for the resistance of K.pneumoniae to FQNs.The qnrA gene that plasmid carried is an important factor for FQNs resistance.
出处
《中国微生态学杂志》
CAS
CSCD
2012年第2期145-148,共4页
Chinese Journal of Microecology
基金
广州市番禺区科技计划资助项目(2007-Z-81-1)
